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Your search keyword '"Alexandr S. Gorbunov"' showing total 2 results
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2 results on '"Alexandr S. Gorbunov"'

1. Apelin Is a Prototype of Novel Drugs for the Treatment of Acute Myocardial Infarction and Adverse Myocardial Remodeling

Author

Sergey V. Popov, Leonid N. Maslov, Alexandr V. Mukhomedzyanov, Boris K. Kurbatov, Alexandr S. Gorbunov, Michail Kilin, Viacheslav N. Azev, Maria S. Khlestkina, and Galina Z. Sufianova

Subjects
heart, ischemia/reperfusion, apelin, adverse remodeling, Pharmacy and materia medica, RS1-441
Abstract

In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is 5–6%. Consequently, it is necessary to develop fundamentally novel drugs capable of reducing mortality in patients with acute myocardial infarction. Apelins could be the prototype for such drugs. Chronic administration of apelins mitigates adverse myocardial remodeling in animals with myocardial infarction or pressure overload. The cardioprotective effect of apelins is accompanied by blockage of the MPT pore, GSK-3β, and the activation of PI3-kinase, Akt, ERK1/2, NO-synthase, superoxide dismutase, glutathione peroxidase, matrix metalloproteinase, the epidermal growth factor receptor, Src kinase, the mitoKATP channel, guanylyl cyclase, phospholipase C, protein kinase C, the Na+/H+ exchanger, and the Na+/Ca2+ exchanger. The cardioprotective effect of apelins is associated with the inhibition of apoptosis and ferroptosis. Apelins stimulate the autophagy of cardiomyocytes. Synthetic apelin analogues are prospective compounds for the development of novel cardioprotective drugs.

Published
2023
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2. Physiological and Pathological Role of TRPV1, TRPV2 and TRPV4 Channels in Heart

Author

Leonid N. Maslov, Alla A. Boshchenko, Alexandr S. Gorbunov, Amteshwar Singh Jaggi, Nirmal Singh, Vladimir V. Bezuglov, Ali Roohbakhsh, Luciano De Petrocellis, and Peter R. Oeltgen

Subjects
0301 basic medicine, TRPV4, medicine.medical_specialty, Ischemia, Cardiomyopathy, TRPV Cation Channels, cardiomyocytes, 030204 cardiovascular system & hematology, Calcitonin gene-related peptide, Article, Pathogenesis, Contractility, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, business.industry, Dilated cardiomyopathy, Heart, General Medicine, Hypoxia (medical), medicine.disease, TRPV1, TRPV2, 030104 developmental biology, Endocrinology, medicine.symptom, Cardiology and Cardiovascular Medicine, business, cardiomyopathy
Abstract

Transient receptor potential vanilloid channel 2 (TRPV2) is required for normal cardiac contractility. The stimulation of TRPV1 in isolated cardiomyocytes can aggravate the effect of hypoxia/ reoxygenation (H/R) on H9C2 cells. The knockout of the TRPV1 gene promotes increased tolerance of the isolated perfused heart to the impact of ischemia/reperfusion (I/R). However, activation of TRPV1 increases the resistance of the heart to I/R due to calcitonin gene-related peptide (CGRP) release from afferent nerve endings. It has been established that TRPV1 and TRPV2 are involved in the pathogenesis of myocardial infarction and, in all likelihood, ensure the cardiac tolerance to the ischemia/reperfusion. It has also been documented that the activation of TRPV4 negatively affects the stability of cardiomyocytes to the H/R. The blockade of TRPV4 can be considered as a new approach to the prevention of I/R injury of the heart. Studies also indicate that TRPV1 is involved in the pathogenesis of cardiac hypertrophy and that TRPV2 channels participate in the pathogenesis of dilated cardiomyopathy. Excessive expression of TRPV2 leads to chronic Ca2+- overload of cardiomyocytes, which may contribute to the development of cardiomyopathy.

Published
2018
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